Zarri I, Bucossi G, Cupello A, Rapallino M V, Robello M
Centro di Neurofisiologia Cerebrale, CNR, Genova, Italy.
Neurosci Lett. 1994 Oct 24;180(2):239-42. doi: 10.1016/0304-3940(94)90529-0.
The effect of nitric oxide (NO) on the function of GABAA receptors was studied in two different rat brain neuron populations. Cerebral cortex neuronal GABAA receptors were studied by preparing microsacs and evaluating 36Cl- accumulation. Whether nitric oxide was provided by sodium nitroprusside (SNP) or by the metabolic precursor precursor arginine there was a 15-25% reduction in the Vmax for GABA-stimulated 36Cl- accumulation. The arginine effect could be reversed by the NO synthase (NOS) inhibitor N omega-nitro-L-arginine. GABAA receptor mediated Cl- currents were studied in rat cerebellar granule cells by whole-cell patch clamp. S-Nitroso-N-acetylpenicillamine (SNAP), sodium nitroprusside and L-arginine reduced the Cl- current elicited by 10 microM GABA. The L-arginine effect was reversible upon its washing out. This circumstance indicates that NO produced by endogenous NOS can inhibit GABAA receptor function in cerebellar granule cells.
在两种不同的大鼠脑神经元群体中研究了一氧化氮（NO）对GABAA受体功能的影响。通过制备微囊并评估³⁶Cl⁻积累来研究大脑皮质神经元的GABAA受体。无论一氧化氮是由硝普钠（SNP）提供还是由代谢前体精氨酸提供，GABA刺激的³⁶Cl⁻积累的最大反应速度（Vmax）都会降低15%-25%。精氨酸的作用可被一氧化氮合酶（NOS）抑制剂Nω-硝基-L-精氨酸逆转。通过全细胞膜片钳技术在大鼠小脑颗粒细胞中研究了GABAA受体介导的Cl⁻电流。S-亚硝基-N-乙酰青霉胺（SNAP）、硝普钠和L-精氨酸降低了由10微摩尔GABA引发的Cl⁻电流。L-精氨酸洗脱后其作用可逆。这种情况表明内源性NOS产生的NO可抑制小脑颗粒细胞中GABAA受体的功能。
